Medical Image of the Week: PSG Sweat Artifact

Figure 1. A 30 second epoch suggestive of sweat artifact and incidentally noted snore artifact on the M1 channels.

Figure 2: Sweat artifact as seen in a 10 second epoch.

Figure 3.  30 second epoch after removal of the M1 channels.

A 61-year-old man, with a past medical history significant for hypertension, COPD and morbid obesity with a body mass index (BMI) of 45.81 is referred for an overnight sleep study for suspicion of obstructive sleep apnea. Artifact was noted on the polysomnogram recording as shown above (Figures 1-3).

Sweat artifact is characterized by slow undulating movement of the baseline recording in the affected channels due to perspiration altering the potential of the involved electrodes (1). Sweat artifact may mimic delta waves and scored as non-rapid eye movement (NREM) stage 3 sleep. Lowering the room temperature, using a fan on the scalp or replacing the conductive paste on the electrodes may help eliminate the artifact.

Safal Shetty, MD¹ and John Roehrs, MD²

¹Banner University Medical Center Tucson, AZ

²Southern Arizona VA Health Care System

Tucson, AZ

Reference

1. Siddiqui F, Osuna E, Walters AS, Chokroverty S. Sweat artifact and respiratory artifact occurring simultaneously in polysomnogram. Sleep Med. 2006;7(2):197-9. [CrossRef] [PubMed] 

Cite as: Shetty S, Roehrs J. Medical image of the week: PSG sweat artifact. Southwest J Pulm Crit Care. 2015;11(4):171-2. doi: http://dx.doi.org/10.13175/swjpcc097-15 PDF 

Medical Image of the Week: DBS Polysomnogram Artifact

Safal Shetty, MD

Kenneth S. Knox, MD 

Pulmonary, Allergy, Critical Care & Sleep Medicine

Banner University Medical Center

Tucson, AZ 

Figure 1. Thirty second epoch showing DBS artifact obscuring all recording channels except flow, efforts belts and the EKG channels. 

Figure 2. Ten second epoch showing the electrical artifact due to DBS.

A 79-year-old man with known Parkinson’s disease and status post deep brain stimulator (DBS) implantation underwent an overnight polysomnogram for clinical suspicion of obstructive sleep apnea. Artifact was seen on the polysomnogram recording (Figures 1 & 2).

Patient-related electrical artifacts may be seen from devices such as pacemakers, deep brain stimulators and vagal nerve simulators. Abrupt discontinuation of DBS is associated with a high likelihood of worsening of symptoms in patients with Parkinson’s disease (1). Patients with DBS are most commonly programmed in monopolar mode. Bipolar configuration, forms a short electrical dipole that affects a relatively smaller volume of tissue and generates far less artifact, suggesting that this may be an effective option in a Parkinsonian patient with indications for polysomnography (2).

References

1. Chou KL, Siderowf AD, Jaggi JL, Liang GS, Baltuch GH. Unilateral battery depletion in Parkinson's disease patients treated with bilateral subthalamic nucleus deep brain stimulation may require urgent surgical replacement. Stereotact Funct Neurosurg. 2004;82(4):153-5. [CrossRef] [PubMed]
2. Frysinger RC, Quigg M, Elias WJ. Bipolar deep brain stimulation permits routine EKG, EEG, and polysomnography. Neurology. 2006;66(2):268-70. [CrossRef] [PubMed]

Cite as: Shetty S, Knox KS. Medical image of the week: DBS polysomnogram artifact. Southwest J Pulm Crit Care. 2015;11(4):151-2. doi: http://dx.doi.org/10.13175/swjpcc096-15 PDF

Medical Image of the Week: REM without Atonia

Figure 1. Polysomnogram with thirty-second epoch showing leg movements and relative increase in chin tone during REM sleep.

Figure 2. Polysomnogram with thirty-second epoch demonstrating similar interval of REM without atonia with the addition of sleep-talking.

A 78 year-old man with a past medical history of Parkinson’s disease (PD) presented to the sleep medicine clinic for evaluation of obstructive sleep apnea (OSA). An overnight polysomnogram (PSG) study was consistent with sleep apnea and revealed frequent leg and arm movements and sleep-talking during rapid eye movement (REM) sleep.

REM sleep behavior disorder (RBD) is a parasomnia characterized by repeated episodes of abnormal behavior occurring during REM sleep (1,2). On PSG, REM sleep without atonia is seen while features of “normal REM” such as number of REM periods and REM cycling remain intact (2). RBD emerges most often in the context of alpha-synucleinopathies, and occurs in up to 60% of PD patients (3). The presence of RBD may be an important preclinical symptom prior to the onset of PD. Cases of PD with RBD are associated with a unique phenotype with an older age of onset, longer disease duration, more profound motor disability, and greater degrees of hallucinations and cognitive dysfunction (3). Establishing a safe sleep environment can be of primary importance in patients with RBD as REM without atonia is associated with injurious behavior. Melatonin is effective as a first-line agent in patients with dementia. In non-demented patients without OSA, low-dose clonazepam is the first line intervention and is rarely associated with withdrawal or need for dose escalation (1). Treating concomitant OSA is important adjunctive therapy.

Jared Bartell, Safal Shetty MD, and Kenneth S. Knox MD

University of Arizona Medical Center

Tucson, AZ

References

1. Aurora RN, Zak RS, Maganti RK, Auerbach SH, Casey KR, Chowdhuri S, Karippot A, Ramar K, Kristo DA, Morgenthaler TI; Standards of Practice Committee; American Academy of Sleep Medicine. Best practice guide for the treatment of REM sleep behavior disorder (RBD). J Clin Sleep Med. 2010;6(1):85-95. [PubMed]
2. Schenck CH, Mahowald MW. REM sleep behavior disorder: clinical, developmental, and neuroscience perspectives 16 years after its formal identification in SLEEP. Sleep. 2002;25(2):120-38. [PubMed]
3. Kim YE, Jeon BS. Clinical implication of REM sleep behavior disorder in Parkinson's disease. Parkinsons Dis. 2014;4(2):237-44. [CrossRef] [PubMed]

Reference as: Bartell J, Shetty S, Knox KS. Medical image of the week: REM without atonia. Southwest J Pulm Crit Care. 2015;10(3):147-8. doi: http://dx.doi.org/10.13175/swjpcc022-15 PDF

Medical Image of the Week: Sleep Bruxism

Figure 1. Hypnogram and polysomnographic tracing showing an episode of rhythmic masticatory muscle activity (RMMA) during sleep. RMMA is defined when at least 3 consecutive EMG bursts (frequency 1 Hz) lasting greater than or equal to 0.25 seconds are scored on the masseter and temporalis channels.

Figure 2. Thirty second epoch of polysomnogram showing phasic sleep-bruxism during stage N2 sleep.

A 42 year-old man with a past medical history of insomnia, post-traumatic stress disorder, depression and both migraine and tension headaches was referred for an overnight sleep study. He had presented to the sleep clinic with  symptoms  of obstructive sleep apnea. Medications included sumatriptan, amitryptiline, sertraline, and trazodone. His sleep study showed: sleep efficiency of 58.2%, apnea-hypopnea index  of 33 events per hour, and arousal index of 14.5/hr. Periodic limb movement index was 29.2/hr. The time spent in the sleep stages included N1 (3.6%), N2 (72.5%), N3 (12.9%), and REM (10.9%). Figure 1 is representative of the several brief waveforms seen on his EEG and chin EMG. Sleep bruxism (SB) is a type of sleep-related movement disorder that is characterized by involuntary masticatory muscle contraction resulting in grinding and clenching of the teeth and typically associated with arousals from sleep (1,2).

The American academy of sleep medicine (AASM) criteria for sleep related bruxism diagnosis:

1. The patient reports or is aware of tooth-grinding sounds or tooth clenching during sleep.
2. One or more of the following is present: A. Abnormal wear of the teeth; B. Jaw muscle discomfort, fatigue, or pain and jaw lock upon awakening; and C. Masseter muscle hypertrophy upon voluntary forceful clenching.
3. The jaw muscle activity is not better explained by another current sleep disorder, medical or neurological disorder, medication use, or substance use disorder.

The exact etiology of SB is unknown. It is associated with sleep arousals, genetic factors, stress, anxiety and behavioral factors and medications like selective serotonin receptor inhibitors, tobacco, alcohol and recreational drug use and sleep disordered breathing (2).

The electromyogram (EMG) activity pattern in patients with SB is known as rhythmic masticatory muscle activity (RMMA) and involves the masseter and temporalis muscles in patterns of phasic and/or tonic contractions, most typically during stages N1 and N2 of sleep (2,3). Clinically, bruxism can result in abnormal tooth wear, masseter muscle hypertrophy, reduced salivation, and morning headaches (1,2).

Sleep bruxism has been shown to be strongly associated with tension and migraine headaches (4). Treatment of the underlying sleep disordered breathing with positive airway pressure may eliminate bruxism during sleep (5). Treatment involves oral appliances such as occlusal splints or mandibular advancement devices (2). There is insufficient evidence to support pharmacotherapy in the treatment of sleep bruxism (1).

Jared Bartell¹, Safal Shetty, MD^1,2, and John Roehrs, MD^1,2

¹University of Arizona Medical Center, Tucson, AZ

²Southern Arizona VA Health Care System, Tucson, AZ

References

1. Macedo CR, Macedo EC, Torloni MR, Silva AB, Prado GF. Pharmacotherapy for sleep bruxism. Cochrane Database Syst Rev. 2014;10:CD005578. [CrossRef] [PubMed] 
2. Carra MC, Huynh N, Lavigne G. Sleep bruxism: a comprehensive overview for the dental clinician interested in sleep medicine. Dent Clin North Am. 2012;56(2):387-413. [CrossRef] [PubMed]
3. Valiente López M, van Selms MK, van der Zaag J, Hamburger HL, Lobbezoo F. Do sleep hygiene measures and progressive muscle relaxation influence sleep bruxism? Report of a randomised controlled trial. J Oral Rehabil. 2014 Nov 21. [CrossRef] [PubMed]
4. De Luca Canto G, Singh V, Bigal ME, Major PW, Flores-Mir C. Association between tension-type headache and migraine with sleep bruxism: a systematic review. Headache. 2014;54(9):1460-9. [CrossRef] [PubMed]
5. Oksenberg A, Arons E. Sleep bruxism related to obstructive sleep apnea: the effect of continuous positive airway pressure. Sleep Med. 2002;3(6):513-5. [CrossRef] [PubMed]

Reference as: Bartell J, Shetty S, Roehrs J. Medical image of the week: sleep bruxism. Southwest J Pulm Crit Care. 2015;10(3):140-2. doi: http://dx.doi.org/10.13175/swjpcc016-15 PDF 

Medical Image of the Week: Polysomnogram Artifact

Figure 1. Thirty second polysomnogram epoch showing artifact in lead O1M2 (black arrow).

Figure 1. Ten second polysomnogram epoch showing artifact in lead O1M2 (black arrow).

A 54 year-old man with a past medical history of attention deficit hyperactivity disorder (ADHD), low back pain, and paroxysmal supraventricular tachycardia presented to the sleep laboratory for evaluation of sleep disordered breathing. Pertinent medications include fluoxetine, ambien, and clonazepam. His Epworth sleepiness score was 18. He had a total sleep time of 12 min. On the night of his sleep study, the patient was restless and repeatedly changed positions in bed. 

Figures 1 and 2 show the artifact determined to be lead displacement of O1M2 after the patient shifted in bed, inadvertently removing one of his scalp electrodes. The sine waves are 60 Hz in frequency. Once the problem was identified, the lead was quickly replaced to its proper position.

Jared Bartell¹, Safal Shetty, MD^1,2, and John D. Roehrs, MD^1,2

¹University of Arizona Medical Center

²Southern Arizona VA Health Care System

Tucson, AZ

Reference as: Bartell J, Shetty S, Roehrs JD. Medical image of the week: polysomnogram artifact. Southwest J Pulm Crit Care. 2015;10(2):95-6. doi: http://dx.doi.org/10.13175/swjpcc014-15 PDF

Medical Image of the Week: Cheyne-Stokes Respiration on Overnight Polysomnography

Figure 1. 300 second polysomnogram window showing crescendo-decrescendo pattern of Cheyne-Stokes respiration (solid black arrows). Cycle length is approximately 60 seconds in duration (Outlined black arrows).

A 75 year old man with a significant past medical history of atrial fibrillation, hypertension, complete heart block status-post pacemaker implantation, thoracic aortic aneurysm, and ischemic cardiomyopathy, was referred to the sleep laboratory for evaluation for suspected sleep disordered breathing. The patient had subjective complaints of morning headaches, reported apnea, un-refreshing sleep, nocturnal urination, and intermittent snoring. The diagnostic polysomnogram was significant for periodic breathing, Cheyne-Stokes pattern, with a cycle length that ranged from 60-65 seconds (Figure 1). Oxygen saturation nadir was 79% as measured by pulse oximetry. Electrocardiogram showed a persistently paced rhythm.

Cheyne-Stokes respiration is a periodic breathing pattern characterized by crescendo-decrescendo episodes of respiratory effort that are interspersed between periods of apnea. It is typically seen in individuals with systolic heart failure, but can also be seen in those with intracerebral hemorrhage or infarction. The mechanism for Cheyne-Stokes respiration involves increased central controller gain causing increased central nervous system sensitivity to changes in arterial blood gas PCO₂ and PO₂. Increased circulation time results in circulatory delay between gas exchange occurring at the alveolar capillary membrane and the central chemoreceptors in the medulla. The result is instability in respiration (1).

Ryan Nahapetian, MD, MPH and Sairam Parthasarathy, MD

Pulmonary, Allergy, Critical Care, & Sleep Medicine

University of Arizona, Tucson, AZ

Reference

1. Quaranta AJ, D'Alonzo GE, Krachman SL. Cheyne-Stokes respiration during sleep in congestive heart failure. Chest. 1997;111(2):467-73. [CrossRef] [PubMed]

Reference as: Nahapetian R, Parthsarathy S. Medical image of the week: Cheyne-Stokes respiration on overnight polysomnography. Southwest J Pulm Crit Care. 2014;8(6):328-9. doi: http://dx.doi.org/10.13175/swjpcc055-14 PDF